Comprehensive Management of
Chronic Rhinosinusitis
Based on EPOS 2020
Abdul Qadar Punagi
Rhinosinusitis
Inflamation of the nose and the paranasal sinuses. Characterized by two or more symptoms, one of
which should be either / nasal blockage / congestion/ nasal obstruction or nasal discharge and : facial
pain / pressure and or reduction or loss of smell
Endoscopic : mucopurulent discharge, odema / mucosal obstruction / nasal polys
CT changes : mucosal changes within ostiomeatal complex and or sinuses
≥ 12 weeks
Chronic Rhinosinusitis (CRS)
Entirely Infectious Inflammatory
disease disease
Unifying hypothesis which explains the
pathogenesis of CRS remains elusive
Prof. Kern (USA
Resilience
Prof. Kern (USA Prof.Lund(UK), EPOS 2020; From Bench to Bedside
Prof. Kern (USA
Prof. Kern (USA
CYTOKINE/SITOKIN
Kata sitokin berasal dari bahasa Yunani: cyto, dari bahasa Yunani "κύτος" kytos "lubang, sel" + kines, dari
bahasa Yunani "κίνησις" kinēsis "pergerakan"
Sitokin adalah kategori luas dari protein kecil (~ 5-20 kDa ) yang penting dalam pensinyalan sel. Pelepasan
sitokin memengaruhi perilaku sel di sekitar mereka. Sitokin dapat terlibat dalam pensinyalan autokrin, pensi
nyalan parakrin, dan pensinyalan endokrin sebagai agen imunomodulasi. Perbedaan lebih jelas antara sitokin
dari hormon masih terus diteliti lebih lanjut. Istilah sitokin bisa mencakup kemokin, interferon, interleukin, limfo
kin, dan faktor nekrosis tumor, tetapi umumnya bukan hormon atau faktor pertumbuhan (meskipun beberapa
tumpang tindih dalam terminologi). Sitokin diproduksi oleh berbagai sel, termasuk sel imun seperti makrofag,
limfosit B, limfosit T, dan sel mast, serta sel endotel, fibroblast, dan berbagai sel stroma. [1] [2]
Wikipedia
CYTOKINE/SITOKIN
Abul K. Abbas, et all; Basic immunology, second Ed, 2004
Prof. Kern (USA)
Prof. Kern (USA)
Classification by EPOS
CRSsNP Th1 Inflamation
2012
CRSwNP Th2 Inflamation
Eosinophilic CRS
2020
Non-Eosinophilic CRS
Prof.Lund(UK), EPOS 2020; From Bench to Bedside
Prof.Lund(UK), EPOS 2020; From Bench to Bedside
Classification by EPOS 2020
Anatomic Endotype Examples of
Distribution Dominance Phenotypes
Type 2 AFRS
Localized
Isolated Sinusitis
(Unilateral) Non-type 2
Primary
CRSwNP/eCRS
CRS
Type 2 AFRS
CCAF
Diffuse
(Bilateral)
Non-type 2 Non-eCRS
Prof.Lund(UK), EPOS 2020; From Bench to Bedside
Classification by EPOS 2020
Anatomic Endotype Examples of
Distribution Dominance Phenotypes
Odontogenic
Fungal ball
Localized Local Pathology Tumour …CPS
(Unilateral)
PDC
Mechanical CF
Secondary
CRS
Diffuse GPA
Inflammatory EGPA
(Bilateral)
Immunity Selective
immunodeficiency
Management of CRS
Appropriate Medical Therapy
• Type 2 (eosinophilic)
• AFRS
• ECRS (CRSwNP >)
• CCAD
Surgical (Functional or non Functional Endoscopic Sinus Surgery)
• Reduce Inflmatory Loads
• Restore Ventilation (non-type 2)
• Improved access for drug delivery to mucosa (type 2>)
Direct Surgical
• Anatamical abnormality
• ACP (SfCP, ECP dan SCP??)
• Mucocele
• Dentogen
• Fungal ball
Appropriate Medical Treatment
Glucocorticoid (Topical and Systeminc
Saline Irigation
Low dose long term macrolide
Antibiotics
Risk factor management
Biological treatment
CRSsNP in adult management scheme for ENT-Specialist
Fokkens, Lund, Mullol, Bachert et al. European position paper for rhinosinusitis and nasal polyps 2012. Rhinology Supplement 23.
CRSwNP in adult management scheme for ENT-Specialist
Fokkens, Lund, Mullol, Bachert et al. European position paper for rhinosinusitis and nasal polyps 2012. Rhinology Supplement 23.
nasal corticosteroids can also be used off-label for:
OPERATIF (FESS/ESS)
PhENOTYPEs AND ENDOTYPEs Of RhINOsINusITIs
According to literature, there are 3 inflammatory pathways:
--> These are T-helper 1 (Th-1) driven, T-helper 2 (Th2) driven and T-helper
17 (Th17) driven pathways.
In CRSsNP, inflammation process is :
mainly driven by Th1 cells. There are increased
number of myeloperoxidase-related neutrophils.
Levels of interferon (IFN)-c, interleukin (IL)-2, and
tumor necrosis factor (TNFα) were increased .
Monoclonal Antibodies
Prof. Kern (USA)
ADCC; Antibody-Dependent Cellular/Cell-mediated Cytotoxicity
ADCC requires an effector cell which classically is known to be natural killer (NK
) cells that typically interact with immunoglobulin G (IgG) antibodies. However, ma
crophages, neutrophils and eosinophils can also mediate ADCC, such as eosinop
hils killing certain parasitic worms known as helminths via IgE antibodies
Antibody-dependent cellular cytotoxicity (ADCC), also called antibody-depende
nt cell-mediated cytotoxicity, is an immune mechanism through which Fc rece
ptor-bearing effector cells can recognize and kill antibody-coated target cell
s expressing tumor- or pathogen-derived antigens on their surface.
Abul K. Abbas, et all; Basic immunology, second Ed, 2004
ADCC; Antibody-Dependent Cellular/Cell-mediated Cytotoxicity
Abul K. Abbas, et all; Basic immunology, second Ed, 2004
